SGK1 and SGK3 both upregulate several ion channels, including the epithelial Na+ channel. SGK1 but not SGK3 is under genomic control of adrenal steroids. SGK1-knockout mice (sgk1-/-) are seemingly normal under standard diet, but their ability to retain NaCl is impaired during salt-deficient diet. In SGK3-knockout mice (sgk3-/-) hair growth is strikingly delayed but NaCl excretion is normal. To explore, whether SGK1 and SGK3 could mutually replace each other, we crossed sgk1-/- and sgk3-/- and compared renal electrolyte excretion of the double mutants (sgk1-/-/sgk3-/-) and their wild-type littermates (sgk1+/+/sgk3+/+). Similar as in sgk3-/-, hair growth was delayed in sgk1-/-/sgk3-/-. Blood pressure was slightly, but significantly lower in sgk1-/-/sgk3-/-(102±4 mmHg) than in sgk1+/+/sgk3+/+(114±3 mmHg), a difference maintained in under low and high salt diets. Plasma aldosterone concentration was significantly higher in sgk1-/-/sgk3-/- than in sgk1+/+/sgk3+/+ under control and low-salt diets. During salt depletion, absolute and fractional excretions of Na+ were significantly higher in sgk1-/-/sgk3-/- than in sgk1+/+/sgk3+/+. Thus, sgk1-/-/sgk3-/- share delayed hair growth with sgk3-/- and modestly impaired renal salt retention with sgk1-/-. Double knockout does not substantially compound the phenotype for either property.